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Skin Diseases in Wrestling

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Skin Diseases in Wrestling Skin conditions in wrestling – how to prevent Krisztián Gáspár, MD, PhD Assistant professor University of Debrecen Faculty of Medicine Department of Dermatology Debrecen, Hungary Disclosure • Presenter: Krisztián Gáspár • I have the Relationships with commercial interests: – Advisory Board/Speakers Bureau: none – Funding (Grants/Honoraria): none – Research/Clinical Trials: Eli Lilly, Novartis, Pfizer, Janssen, Sanofi, Abbvie – Speaker/Consulting Fees: Eli Lilly, Novartis, Janssen, Sanofi, Abbvie • None to disclose regarding this presentation Objectives • Normal and impaired skin barrier • Atopic dermatitis – model for understanding barrier • Skin diseases in wrestling • Treatments • Prevention techniques in skin infections Skin barrier Danger model: ”The basic function of immune system is not to distinct between self and non-self, but to recognize danger” Polly Matzinger, PhD, Immunologist, NIH In order to avoid or prevent a loss on the mat you need a good defense – The same is true for skin (an active defense) Skin barrier functions Physicochemical barrier and immunological barrier – in close morphological and functional connection Physicochemical barrier Immunological barrier (SIS) Stratum corneum: corneocytes • Epidermis, dermis Stratum granulosum: keratinocytes • Keratinocytes, dendritic cells, T cells Cornified envelop , structural proteins • Defensins, cytokines, chemokines (filaggrin) Lipid layer, proteases, protease inhibitors, defensins Tight junctions, corneodesmosomes Physicochemical barrier Genetics Environmental factors - microbes (viruses, fungi, bacteria, parasites) - physical factors (e.g. UV, humidity, scratching) - chemicals (e.g. irritants) - biological factors (allergens) http://crmsnchrysnths.blogspot.com/2017/09/what-is-skin-barrier.html Elements of intact physicochemical barrier Barrier: Cells: corneocytes Intercellular junctions: corneodesmosomes Intercellular matrix: lipids, enzymes https://www.sheffield.ac.uk/iicd/research/rr/dermatology/skinbarrierfacility Five major groups of skin barrier genes Enzymes having role in desquamation and cross-linking Tight junction KLK7 KLK5 KLK14 components TGM1 TGM3 TGM5 CLDN1 CLDN16 CLDN23 Barrier structure components OCLN Keratins: Other KRT1 molecules: KRT10 FLG KRT6 LOR Corneodesmosome KRT16 PPL components KRT17 SPRR1A CDH1 DSG1 KRT79 SPRR2A DSC1 PKP1 LCE1F CDSN LCE1D Antimicrobial peptides (AMPs) S100A7 S100A8 S100A9 DEFB4B LCN2 TSLP Impaired physicochemical barrier http://crmsnchrysnths.blogspot.com/2017/09/what-is-skin-barrier.html Current Dermatology Reports December 2018, Volume 7, Issue 4, pp 209–220 Skin Barrier Function and Atopic Dermatitis Consequences of impaired barrier Increased penetration of Increased transepidermal allergens, irritants, pathogens waterloss (TEWL) + increased KC and LC activity that leads to increased immunbarrier activity Inflammation Hudson TJ Nature Genetics 2006 Immunological barrier ADAPTIVE immune response INNATE immune response Slowly developing Antigen specific Immediate reaction Transferrable to Not antigen specific another host Not transferrable No immunmemory Immunmemory exists Exponential empowering Major elements of cutaneous immune responses Innate immune response Adaptive immune response Cellular Phagocytes (macrophages, granulocytes) T lymphocytes elements Dendritic cells B lymphocytes NK cells Keratinocytes Endothelial cells Humoral Complement system Antibodies elements Cytokines Interleukins chemokines (cytokines) C-reactive protein Mannose-binding lectin Lipopolisacharide-binding protein Antimicrobial peptids etc. Skin as an immune organ Resident skin immune cells Impaired immunological barrier Good model of impaired physicochemical and immunological barrier Inflamm Regen. 2017 Jun 5;37:14. doi: 10.1186/s41232-017-0044-7. Pathogenesis of AD Genetic factors (mutations, epigenetics) Close and not independent connection Decreased level of FLG Skin infections, low and structure proteins between the pDC, PMN cell count in skin abnormalities of epidermal Innate and Skin barrier barrier Adaptive changes, dry Immune system skin, mechanic function and changes trauma immunological Sensitization, Proinflammatory cytokines mechanisms, Leukocyte recruitment and chemokines with genetic and activation (TSLP, IL-16, TNFa, CCL26, CCL27) and Hygiene hypothesis – soaps, environmental Hygiene hypothesis – Impaired detergents in barrier impairment Th1/Th2 balance and Treg function changes in the Environmental factors background (allergens, irritants, microbes, stress) Atopic Dermatitis • Chronic, non-contagious inflammatory skin disease. • Dry skin, pruritus, possible superinfections (>90% S. aureus colonization). • Prevalence in Europe in children 15-25%, in adults 2-10%, continuously increasing. Skin barrier prevention – levels of prevention • Primary prevention: healthy person • Secondary prevention: atopic, symptom free (+atopy march) • Tertiary prevention: atopic, chronic patient Prevention techniques – possibilities • Avoidance mechanisms (specific and non- specific triggers, provocation factors) (?) • Diet, probiotics • Continuous emollient use Simpson et al JACI 2014 The First: open-label, prospective study High AD-risk children: 30-50% development of AD in first 2 years 22 high AD-risk newborns Emollient therapy From week 1 for 2 years (2006-2008) Daily at least 1x (QD) 15 % developed disease Transepidermal waterloss (TEWL) decreased Simpson E et al. JAAD 2010 The First: Randomized, controlled study 124 high AD-risk newborns (108 finished study) Emollient therapy (oil, cream, ointment) from M1 for 6 months (2010-2011) Daily at least 1x In control group no emollient Emollient use well tolerated by patients AD cumulative incidence (50% drop): emollient group 22%, control group 44% Therapy adherence high Simpson E et al. JACI 2014 Prospective, randomized, controlled trial 118 high AD-risk newborns Emollient therapy from M1 for 32 weeks (2010-2013) Daily at least 1x In control group no emollient AD cumulative incidence dropped by 33% Horimukai et al. JACI 2014 New clinical studies Higher patient number More frequent use AD incidence? Presence of sensitization? Longer trials Why important to restore the barrier? Basic treatment • Complex treatment in AD is unavoidable and inevitable in both acute and chronic form of disease. • Helps in rehydration of skin, decreasing skin dryness. Replaces essential fatty acids locally. • Increases skin elasticity. Decreases tension and itch of skin. Cleaning effect. • Daily min. 2x in case of symptoms and 1x daily for preventive reasons • Whole body use Emollient therapy in AD • Emollients right after shower (~5 min; ~27 Celsius), after gentle drying (skin still moist). • Long effect even without shower. • Allergens in emollients must be avoided to prevent sensitization via skin. • By its water-binding elements (e.g. urea, glycerol, hyaluronic acid) it hydrates stratum corneum • Occlusive characters (lipid, fat, oil contain) TEWL decreases • Further effects: changes microbiome and pH; increases AMP level; FLG and loricrin expression increases; T cell and DC infiltration decreases; antifungal, anti-pruritic, anti-inflammatory effects FLG: filaggrin; TEWL: transepidermal waterloss; AMP: antimicrobial peptide Wollenberg és mtsai 2003; Boussault és mtsai 2007; Chiang & Eichenfield, 2009 Skin diseases in wrestling • Trauma • Eczema (contact dermatitis) • Infection (fungal, bacterial, viral, parasitic) Contact dermatitis • Heterogeneous group • Noninfectious inflammatory dermatoses in which the the pathological changes in the epidermis and the upper dermis produce distinctive clinical pictures • Extremely common, 15-25% of patients with skin diseases • Occupational dermatosis (No1) Classification of eczemas Exogenous agents and Exogenous agents genetic susceptibility Dermo-epidermal Dermo-epidermal barrier Id-reaction barrier and immunological mechanisms Irritant Allergic contact Asteatotic eczema contact dermatitis dermatitis Dyshidrosis Chronic cummulative Mikrobial eczema irritant eczema Hyperkeratotic Nummular eczema handand foot eczema Pityriasis simplex Seborrheic eczema Dermatitis glutealis Atopic dermatitis infantum Intertrigo Intertriginosus eczema Special forms Treatments in general • Conventional medicine must be recommended and prescribed by physicians or health care professionals. • Wrestlers not reporting a skin condition/infection and using unusual and unhealthy treatments (e.g. nail polish remover, bleach, salt, vinegar solutions) are causing unwanted adverse events (e.g. suffocate or burn an infection, leaving extensive scars). • ”Home remedies” – may be successful, but do not guarantee to kill the infection (only eliminating visible symptoms temporarily). Thus infections may not be symptomatic, but still remain transmittable. Contact dermatitis – treatment • Define etiology, classification • Eliminate provoking factors • Restore epidermal barrier function • Moisturize • Anti-inflammatories, immunosuppression (topical corticosteroids, topical calcineurin inhibitors) Acronym: DERMA (skin) Skin infections in wrestling 10% of time-loss injuries in wrestling are due to skin infections By National Collegiate Athletic Association's (NCAA) Injury Surveillance System • Fungal • Bacterial • Viral • Parasitic • Overall skin infection rate 14/10000 • 22% recurrence rate • Rate for viral infections was 1.7x the rate of bacterial and 2.1x the rate of fungal infections NCAA GUIDELINE 2j Skin Infections in Athletics 2008 Herzog MM et al J Athletic Training 2017; 52:457-63. Skin infections
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